Cases reported "Epilepsy"

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11/21. CT findings following diphenylhydantoin intoxication.

    CT findings in three female epileptic patients are presented. The patients were treated with toxic doses of the anticonvulsant diphenylhydantoin, leading to irreversible ataxia of varying severity. CT shows cerebellar atrophy, including discernible sulci, a dilated 4th ventricle, basal cisterns, and subarachnoid space. These effects of severe DPH toxicity are relevant in the differential diagnosis of 'idiopathic' and other toxic and systemic atrophies, as well as dysontogenetic lesions of the cerebellum.
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ranking = 1
keywords = intoxication
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12/21. Transient hyperkinesia after a single intravenous perfusion of diphenylhydantoin. Report of a case associated with nontoxic plasma levels of diphenylhydantoin.

    Transient hyperkinesia was observed in a 16-year-old epileptic and mentally retarded patient after a single intravenous perfusion of diphenylhydantoin (DPH). No clinical signs of DPH intoxication were associated with the movement disorder. Repeated plasma anticonvulsant level determinations never showed toxic concentrations of DPH. Since a few spontaneous episodes of hyperkinesia had been observed before, the DPH intravenous perfusion could have unmasked a preexisting latent movement disorder in our patient. However, neuroradiological investigations failed to demonstrate the existence of any anatomical damage of the basal ganglia, and HVA as well as 5-HIAA levels measured in the CSF with the probenecid technique were within the normal range 2 months after cessation of hyperkinesia. HVA and 5-HIAA levels have also been measured in the CSF during the period with hyperkinesia; the results are discussed with reference to previously published data concerning cerebral monoamine metabolism in drug-treated epileptic patients.
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ranking = 0.25
keywords = intoxication
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13/21. phenytoin-related cerebellar degeneration without seizures.

    Cerebellar changes have been reported in relationship to epilepsy alone as well as to phenytoin therapy for the control of seizures. The cliniconeuropathological correlation between these changes and epilepsy or the anticonvulsant is usually complicated by the presence of both variables. Experimental evidence suggests that phenytoin alone may be sufficient to cause cerebellar changes following intoxication. We report a case of cerebellar degeneration in a patient treated with isoniazid and prophylactically treated wtih phenytoin who never had a seizure.
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ranking = 0.25
keywords = intoxication
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14/21. Antiepileptic drugs and psychiatric disorders: mechanism involved in manifestation of psychic symptoms of high blood level of antiepileptics.

    The adverse psychic effects of antiepileptics embrace all categories of psychiatric symptomatology, including disturbances of consciousness (delirium, confusion), psychotic state (schizophrenia-like psychosis, affective disorder), neurotic state, behavior and character disorder. Antiepileptic intoxication can take the form of a psychotic episode. The lowered level of consciousness due to a high blood level of antiepileptics is expressed as inhibitory symptoms such as a lack of initiative, psychomotor slowing, lowering mood, stuporous state and the like. Another group of manifestation of a high blood level of antiepileptics, by contrast, consists of salient positive symptoms such as irritability, hyperkinetic syndrome, hysterical symptoms, aggravation of character change, delirium and confusion. An elevated blood level of antiepileptics by itself is not sufficient to give rise to a psychiatric symptom, which is rather prone to occur in the presence of some trouble or problems (defect in intelligence or personality, fragility of brain function, organic brain damage, psychogenic factors) in the patient.
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ranking = 0.25
keywords = intoxication
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15/21. Pontoneocerebellar hypoplasia--a probable consequence of prenatal destruction of the pontine nuclei and a possible role of phenytoin intoxication.

    The autopsy findings of a 21/2-year-old microcephalic, mentally retarded girl, with tetraparesis, and dysmorphic features are reported. Neuropathologic findings, typical of the ponto-neocerebellar hypoplasia described by Brun [1917], suggest that this abnormality was the result of a prenatally acquired destruction of the pontine nuclei, with a secondary retrograde degeneration of the dentatopontine tract. The possible role of phenytoin, taken by the mother during pregnancy, is discussed.
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ranking = 1
keywords = intoxication
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16/21. Van Gogh's vision. digitalis intoxication?

    Vincent van Gogh, the Dutch postimpressionist painter, died in 1890. He was an uncommon man. Automutilation, depression, insanity, and suicide are part of his medical history. During the last few years of his life, his paintings were characterized by halos and the color yellow. Critics have ascribed these aberrations to innumerable causes, including chronic solar injury, glaucoma, and cataracts. Van Gogh may have been under the influence of digitalis intoxication and its side effects: xanthopsia and coronas. This hypothesis is based on his twice having painted his physician holding a foxglove plant; that this medicine was used in the latter part of the 19th century in the treatment of epilepsy; and that the toxic effects of digitalis may have, in part, dictated the artist's technique.
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ranking = 1.25
keywords = intoxication
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17/21. Choreo-athetosis induced by phenytoin in an epileptic child. A case report.

    A 5-year-old child with epilepsy and underlying brain damage developed choreo-athetosis during intoxication with phenytoin. Drug intoxication was suggested by the dose the child was taking (75 mg 3 times a day) and confirmed by measuring the serum phenytoin concentration which was 229 mmol/l (therapeutic range 40-80 mmol/l). The choreoathetoid movements ceased 4 weeks after discontinuation of the drug, although the blood level returned to the therapeutic range after 2 weeks.
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ranking = 0.5
keywords = intoxication
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18/21. Fictitious epilepsy in munchausen syndrome by proxy: family psychodynamics.

    This paper presents experience of munchausen syndrome by proxy in four families where symptoms and signs of seizures in children were deliberately fabricated or induced by their own parent. At the time when the condition was suspected, the children (5, 7, 13 and 14 years old) had already been exposed to numerous investigations and antiepileptic drug intake-in one case resulting in drug intoxication. The important data, giving clues about how to uncover the condition, are peculiar to each family. After the condition was confirmed, a multidisciplinary team organized an approach aimed at protecting the abused child and changing the pathological parent-child relationship. personality disorders were recognized in all illness perpetrators (the father in one and the mother in three families) and various psychopathological manifestations were present in all of the abused children. Psychodynamic factors causing the Manchausen Syndrome by Proxy are described and discussed.
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ranking = 0.25
keywords = intoxication
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19/21. Epileptic seizure associated with intracerebroventricular and intrathecal morphine bolus.

    We report on two patients with morphine-related seizures associated with either intrathecal or intracerebroventricular administration. Both patients had a history of malignant tumor and both experienced the seizures following bolus application of morphine, while even higher dosages were well tolerated when continuously infused. seizures occurred without signs of intoxication. Initiation of intrathecal morphine therapy and bolus application should be performed carefully and only when constant monitoring is provided for at least 12 h. Animal data and possible mechanisms for morphine-related seizures are discussed.
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ranking = 0.25
keywords = intoxication
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20/21. carbamazepine intoxication with negative myoclonus after the addition of clobazam.

    We report a case a carbamazepine (CBZ) intoxication with negative myoclonus that occurred 4 weeks after clobazam (CLB) had been added to a stable regimen of CBZ and topiramate (TPM). Both CBZ and CBZ-epoxide (CBZ-E) blood levels were elevated, and the symptoms resolved quickly when CBZ dosage was reduced and CLB discontinued. CLB was reintroduced a year later with the patient's consent, and the time course of the interaction was studied: CBZ and CBZ-E levels increased slowly over 12 days. The interaction is thus probably related to the progressive increase in Nor-CLB.
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ranking = 1.25
keywords = intoxication
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